PURPURA SCHÖNLEIN-HENOCH CU MANIFESTĂRI NEUROLOGICE

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1 9 PREZENTĂRI DE CAZ PURPURA SCHÖNLEIN-HENOCH CU MANIFESTĂRI NEUROLOGICE Georgeta Diaconu 1, Ioana Grigore 1, Dana Anton 1, Laura Trandafir 1, M. Burlea 2 1 Clinica a III-a Pediatrie, 2 Clinica a V-a Pediatrie, Spitalul Clinic de Urgenţe pentru Copii Sf. Maria, Iaşi 2 Universitatea de Medicină şi Farmacie Gr. T. Popa Iaşi REZUMAT Simptomele neurologice reprezintă manifestări posibile ale purpurei Schönlein-Henoch. Autorii prezintă doi copii diagnosticaţi cu purpură Schönlein-Henoch la care semnele de debut au fost neurologice, fi ind reprezentate de crize epileptice. În ambele cazuri s-au asociat tulburări de comportament, iar EEG intercritic a evidenţiat grafoelemente patologice. Într-un caz examenul neuroimagistic cerebral a obiectivat leziuni ischemice cerebrale. Autorii confi rmă că purpura Schönlein-Henoch poate interesa sistemul nervos, iar revederea literaturii arată că cele mai frecvente manifestări neurologice ale acestei boli sunt crizele epileptice şi tulburările de comportament, urmate de cefalee, defi cite neurologice focale, mononeuropatii şi poliradiculoneuropatii. Cuvinte cheie: purpură Schönlein-Henoch, crize epileptice, tulburări de comportament Purpura Schönlein-Henoch este cea mai importantă vasculită a copilului, atât prin frecvenţă, cât şi prin variabilitatea tabloului clinic, care poate merge de la forme paucisimptomatice cu evoluţie rapidă şi benignă la forme grave recidivante cu prognostic rezervat. Boala debutează frecvent în mica copilărie, dar poate apărea la orice vârstă, remarcându-se o incidenţă mai mare la sexul feminin, raportul pe sexe fiind de 2/1 (McCarthy, 2010). Apariţia simptomatologiei este în general precedată de o infecţie intercurentă de căi respiratorii, incidenţa purpurei fiind mai mare în sezonul rece. În majoritatea cazurilor afecţiunea este autolimitantă, având evoluţie favorabilă în decurs de maximum o lună, deşi în 1/3 din cazuri pot exista recăderi (Saulsbury 2007, Kellerman 2006). Etiologia purpurei Schönlein-Henoch nu este pe deplin înţeleasă, dar se presupune că anumiţi factori triggers acţionează ca antigene, determinând activarea căii alternative a complementului, iar markerii genetici determină predispoziţia pentru boală şi influenţează severitatea acesteia (Brogan, 2007). Manifestările neurologice, în general rare, pot face parte din tabloul clinic al bolii şi sunt considerate consecinţa unei vasculite cerebrale sau a hemo ragiei subarahnoidiene. Cefaleea şi tulburările de comportament sunt raportate la un număr semnificativ de copii cu purpură Schönlein-Henoch, însă simptomele neurologice severe sunt în general rare în faza acută a bolii (Bakkaloğlu, 2000). Autorii prezintă doi copii la care manifestările neurologice au reprezentat semnele de debut în purpura Schönlein-Henoch. CAZ 1 RV, 5 ani şi 9 luni, sex feminin, născută la termen din părinţi neconsanguini, după o sarcină cu evoluţie normală, cu greutatea la naştere de g şi scor Apgar 8, ajunge în observaţia noastră la vârsta de 4 ani şi 10 luni pentru 2 crize focale cu semiologie mo to rie manifestate prin clonii la nivelul hemicorpului stâng, cu devierea globilor oculari şi comisurii bu cale de aceeaşi parte. Anamnestic, dezvoltarea neuropsihomotorie a copilului a fost normală pe etape de vârstă şi antecedentele familiale au fost negative pentru afecţiuni neurologice. Examenul clinic general la internare a relevat dezvoltare somatică armonioasă, TA = 90/50 mmhg, puls = 88/min. Examenul neurologic obiectiv nu a relevat sem ne de deficit focal sau de hipertensiune intracraniană. Adresa de corespondenţă: Dr. Ioana Grigore, Clinica III Pediatrie, Spitalul Clinic de Urgenţe pentru Copii Sf. Maria, Str. Vasile Lupu, nr. 62, Iaşi, cod REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN 2012

2 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN Pacienta prezenta intelect normal (QI = 85) şi periodic agitaţie psihomotorie cu deficit de atenţie şi toleranţă scăzută la frustrare. Bilanţul hematologic şi biochimic sanguin a fost în limite normale. Examenul EEG intercritic a obiectivat descărcări focale de vârfuri difazice şi complexe vârf-undă lentă în regiunile temporo-parietale (Figura 1). CT-scan cerebral a relevant craniu cu formă, dimensiuni, structuri osoase, suturi şi cavităţi pneumatice conforme cu vârsta, substanţa cerebrală şi spaţiile lichidiene cu morfologie, densitate şi priză de contrast în limite normale. Electro-clinic, pacienta a fost diagnosticată cu epilepsie cu crize parţiale motorii şi a primit tratament cu oxcarbazepină 450 mg/zi. Copilul revine după o săptămână pentru dureri abdominale difuze însoţite de senzaţie de greaţă şi vărsături şi apariţia unei erupţii cutanate purpurice. Examenul clinic general a evidenţiat leziuni pur purice dispuse simetric pe suprafaţa extensorie a membrelor inferioare şi fese, care se accentuau în clinostatism. Examenele de laborator au evidenţiat o creştere moderată a reactanţilor de fază acută (VSH=35 mm/h, proteina C reactivă prezentă) şi a IgA serice (298 mg/dl), titrul ASLO fiind de 800 UI. Testele de coagulare şi numărul de trombocite au fost normale. Examenul de urină repetat a fost normal. Exudatul faringian a evidenţiat prezenţa streptococului β hemolitic gru pa A. Pacienta a fost diagnosticată cu purpură Schönlein-Henoch cu debut neurologic. Tratamentul a constat în administrarea de Penicilină G timp de 10 zile, continuarea medicaţiei antiepileptice în aceeaşi doză şi repaos la pat. Evoluţia a fost favorabilă, cu remiterea simptomatologiei cutanate în 3 săptămâni. Pacienta nu a mai prezentat crize epileptice. CAZ 2 MA, 11 ani, sex masculin, născut la termen cu g şi scor Apgar 9 după o sarcină normală, ajunge în observaţia noastră la vârsta de 9 ani şi 11 luni pentru crize generalizate tonico-clonice însoţite FIGURA 1. EEG intercritic: descărcări focale de vârfuri difazice şi complexe vârf-undă lentă în derivaţiile temporo-parietale

3 396 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN 2012 de pierderea conştienţei şi tulburări vegetative, de scurtă durată, cu debut de dată recentă. Intercritic, pacientul prezenta episoade de cefalee difuză, iritabilitate marcată, cu scăderea toleranţei la frustrări minore, senzaţie de greaţă, vărsături şi dureri abdominale colicative intermitente, simptome ce au debutat la 2 săptămâni după o infecţie virală intercurentă a căilor respiratorii superioare. Anamnestic, datele familiale şi personale au fost negative pentru afecţiuni neurologice. Examenul clinic general a relevat dezvoltare staturo-ponderală normală, TA=100/60 mmhg, puls =78/min, dureri abdominale difuze, intermitente. Examenul neurologic obiectiv a fost normal. Intercritic, pacientul prezenta cefalee difuză cu iritabilitate marcată şi toleranţă scăzută la frustrări minore cu heteroagresivitate. Traseul EEG spontan a fost normal, dar s-au evidenţiat descărcări generalizate de complexe vârfundă lentă la probele de activare (Figura 2). Examenul neuroimagistic a evidenţiat accident vascular ischemic în teritoriul arterelor cerebrale mijlocii stângi (Figura 3). Ecografia abdominală a fost normală. Examenul chirurgical a exclus un abdomen acut chirurgical. Pacientul a fost diagnosticat cu accident vascular cerebral ischemic şi epilepsie generalizată simptomatică, pentru care a primit tratament cu valproat de sodiu 600 mg/zi. La 10 zile de la internare a apărut o erupţie purpurică localizată simetric, metameric, la nivelul membrelor inferioare şi fese. Examenele de laborator au evidenţiat creşterea reactanţilor de fază acută (VSH=55mm/h, proteina C reactivă prezentă), ASLO 600 UI. Bilanţul funcţional hepatic şi renal a fost în limite normale. FIGURA 3. CT-scan cranio-cerebral: arie hipodensă extinsă localizată temporo-fronto-parietal stâng în teritoriul arterei cerebrale mijlocii stângi, cu minim efect de masă pe ventriculul lateral stâng Exudatul faringian a evidenţiat streptococ β hemolitic grupa A. Pacientul a fost diagnosticat cu purpură Schönlein-Henoch şi crize epileptice generalizate tonicoclonice şi a primit tratament cu Penicilină G, antiinflamatorii nesteroidiene şi medicaţie antiepileptică. Evoluţia clinică a fost favorabilă, copilul fiind în prezent fără crize. FIGURA 2. EEG: descărcări generalizate de complexe vârf-undă lentă la hiperpnee

4 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN DISCUŢII Purpura Schönlein-Henoch este o vasculită generalizată caracterizată prin leziuni cutanate, dureri articulare, semne gastrointestinale şi renale. În general, simptomele sunt mai severe la copiii mai mari (Watson, 2012). Manifestările neurologice pot să apară ocazional, majoritatea sunt de gravitate medie, fiind reprezentate de cefalee şi tulburări de comportament. Simptomele neurologice severe pre - cum crize epileptice, neuropatii periferice, hemoragii intracerebrale şi encefalopatii sunt rar întâlnite în purpura Schönlein-Henoch (Østergaard 1991, Elinson 1990). Substratul patogenic al manifestărilor neurologice din purpura Schönlein-Henoch se presupune că este reprezentat de leziuni de vasculită cerebrală. Într-un studiu din 2009 realizat pe un lot reprezentativ de 430 de copii diagnosticaţi cu purpură Schönlein-Henoch, Anil şi colaboratorii raportează prezenţa semnelor neurologice la 0,7% din cazuri. Østergaard (1991) a raportat prezenţa descărcărilor EEG focale la mai mult de 50% dintre copiii urmăriţi cu purpură Schönlein-Henoch, chiar dacă nu aveau simptomatologie neurologică. Elinson (1990) a remarcat prezenţa la examenul neuro imagistic a unor semne de ischemie cerebrală la bolnavii cu purpură Henoch-Schönlein. Într-un număr redus de cazuri s-au raportat la pacienţii cu purpură Henoch-Schönlein şi crize epileptice, iar prezenţa la examenul neuroradiologic a hemoragiei intracerebrale se presupune că se datorează vasculitei cerebrale, fiind atribuită reducerii nivelului de protrombină şi de factor XIII (Mirsa 2004, Karamadoukis 2008). Ambele cazuri cu purpură Schönlein-Henoch prezentate în lucrare s-au caracterizat prin afectarea concomitentă a mai multor organe şi sisteme. Este posibil ca streptococul β hemolitic grupa A să fi avut un potenţial rol patogenic la cei doi pacienţi evaluaţi. În ambele situaţii simptomele neurologice (crizele epileptice, tulburările de comportament, ce faleea) au debutat înainte de apariţia semnelor cutanate specifice purpurei Schönlein-Henoch. Explorarea neuroimagistică a fost normală la un pacient, dar la al doilea s-au obiectivat leziuni ischemice cerebrale. Examenul EEG a relevat gra fo - elemente patologice la ambii copii. Evoluţia pacienţi lor a fost favorabilă, crizele epileptice fiind con - trolate complet de medicaţia antiepileptică. CONCLUZII Purpura Schönlein-Henoch este o afecţiune multisistemică din al cărei tablou clinic pot face parte şi manifestările neurologice. Crizele epileptice şi tulburările de comportament intercritice au fost prezente la ambii copii evaluaţi, reprezentând în ambele cazuri semnele de debut ale purpurei Schönlein-Henoch. Evoluţia manifestărilor neurologice a fost favorabilă, medicaţia antiepileptică controlând complet crizele epileptice la cei doi pacienţi. Schönlein-Henoch purpura with neurological manifestations Georgeta Diaconu 1, Ioana Grigore 1, Dana Anton 1, Laura Trandafir 1, M. Burlea 2 1 3rd Clinic of Pediatrics, 5th Clinic of Pediatrics 2 University of Medicine and Pharmacy Gr.T. popa, Iasi ABSTRACT Neurological symptoms represent possible manifestations of Schönlein-Henoch purpura. The authors present two children diagnosed with Schönlein-Henoch purpura. In booth cases the onset of disease was with neurological symptoms (epileptic seizures). In booth cases was observed behavioral problems and interictal EEG revealed abnormalities. In one case the neuroimaging exam revealed cerebral ischemic lesions. The authors consider that Schoenlein-Henoch purpura can involve the nervous system and review of the literature indicates that epileptic seizures and behavioral changes are the most frequent neurologic manifestations of this disease, followed by headache, focal neurologic defi cits, mononeuropathies and polyradiculoneuropathies. Key words: Schönlein-Henoch purpura, epileptic seizures, behavioral problems Schönlein-Henoch purpura is the most important of the child vasculitis, both by frequency and by the variability in the clinical picture that can go from rapidly evolving forms with benign prognosis to serious and recurrent forms with reserved prognosis. The disease begins often in small childhood,

5 398 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN 2012 but can occur at any age, with high incidence on female, sex ratio of 2/1 (McCarthy, 2010). The appearance of the symptomatology is generally preceded by an intercurrent respiratory infection, the incidence of the disease being higher in the winter season. In most cases the condition is self-limited with favorable evolution within a maximum of one month, although in 1/3 of cases there may be relapses (Saulsbury 2007, Kellerman 2006). The etiology of Schönlein-Henoch purpura is not fully understood, but it is believed that several factors act as triggers causing antigens alternative complement pathway activation and determine genetic markers for disease susceptibility and severity influence. The etiology of Schönlein-Henoch purpura is not fully understood, but it is assumed that certain factors act as triggers causing activation of the alternative pathway of complement and the genetic markers determine susceptibility for disease and influence the severity of it (Brogan, 2007). Neurological manifestations generally rare, can be part of the clinical picture of the disease and are considered to be the consequence of an cerebral vasculities or subarachnoid hemorrhage. Headache and behavior disorders are reported to a significant number of children with Henoch-Schönlein purpura, but severe neurological symptoms are generally rare in the acute phase of the disease (Bakkaloğlu, 2000). The authors present two children who had neurological signs at the Schönlein-Henoch purpura onset. CASE 1 RV, 5 years 9 months, female, born from parents who were not related, after a pregnancy with normal evolution, weight at birth 3,700 g and Apgar score 8, arrives in our observation at the age of 4 years 10 months for 2 seizures with focal motor semiology manifested with clones movements of the left side of the body with deviation to left of the eyes and deviation of the corner of mouth to the same side. Child neurological development was normal on the stages of age and family history was negative for neurological disorders. General clinical examination on admission revealed the harmonious somatic development, TA = 90/50 mmhg, pulse = 88/min. FIGURE 1. Interictal EEG: focal spike and spike-slow wave complex in temporo-parietal regions

6 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN Objective neurological examination was not relevant focal deficit or signs of intracranial hypertension. Patient had normal intellect (QI = 85) and periodically psychomotor agitation with attention deficit and low frustration tolerance. Hematological and blood biochemical balance was normal. EEG examination objectified downloads of focal spike and spike-slow wave complex in temporo-parietal regions (Figure 1). CT brain scan revealed skull shape, size, bone structure, sutures and air cavities in accordance with age, substance cerebral and fluid spaces with morphology, density and outlet contrast in normal range. Patient was diagnosed with partial seizures epilepsy and received treatment with oxcarbazepine 450 mg/day. The child returns after a week to diffuse abdominal pain accompanied by nausea and vomiting feeling and appearance of a purpuric rash. General clinical examination revealed purpuric lesions symmetrically arranged on the expander surface of lower limb and buttocks, which is which is emphasized in supine. Laboratory testing revealed a moderate increase of acute phase reactants (VSH = 35 mm/h, C-reactive protein present) and serum IgA (298 mg/dl), the titer ASLO being 800 UI. Coagulation tests and platelet counts were normal. Repeated urine examination was normal. Pharyngeal exudate showed the presence of β hemolytic streptococcus type A. The patient was diagnosed with Henoch-Schönlein purpura with neurological onset. The treatment consisted in the administration of penicillin G for 10 days, continuing in the same dose of anti-epileptics drugs and rest in bed. Evolution was favorable with skin symptoms have resolved in 3 weeks. The patient has not presented the epileptic seizures. CASE 2 MA, 11 years old, male, born at term with 2,800 g, Apgar score 9 and after a normal pregnancy, arrives in our observation at the age of 9 years 11 months for generalized tonic-clonic seizures accompanied by loss of consciousness and vegetative manifestations, with brief recent onset. Interiactal patient present episodes of diffuse headache, marked irritability with decreasing tolerance to minor frustrations, feeling nausea, vomiting and intermittent colicky abdominal pain, and symptoms started 2 weeks after a viral infection of the upper respiratory tract. Personal and familial history was negative for neurological disorders. General clinical examination revealed normalweight development, TA = 100/60 mmhg, pulse = 78 rpm, diffuse, intermittent abdominal pain. Objective neurological examination was normal. Interictal patient present diffuse headache and marked irritability with the low tolerance in minor frustrations with aggression. FIGURE 2. EEG: generalized complex of spike-slow wave at activation tests

7 400 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN 2012 The spontaneous EEG was normal, but had revealed downloads of generalized complex of spikeslow wave at activation tests (Figure 2). Neuro-imagistic examination showed ischemic cerebral stroke in the territory of the left middle arteries (Figure 3). Abdominal echografie was normal. FIGURE 3. CT-scan: hypodense area extended on left fronto-temporo-parietal located in the left middle cerebral artery territory with minimal effect of mass on left ventricular Surgical examination excluded a surgical acute abdomen. The patient was diagnosed with transient ischemic strokes and symptomatic generalized epilepsy, for which he received treatment with sodium valproate 600 mg/day. To 10 days after admission there was a purpuric eruption symmetrically located, on the legs and buttocks. Laboratory testing revealed increase in acute phase reactants (VSH = 55 mm/h, C-reactive protein present), ASLO 600 IU. Hepatic and renal functional balance was normal. Pharyngeal exudate showed the presence of β hemolytic streptococcus type A. Patient was diagnosed with Henoch-Schönlein purpura and generalized tonic-clonic epileptic seizures and received treatment with Penicillin G, steroidal anti-inflammatory medication and antiepileptic drugs. Clinical evolution was favorable, the children being in present without seizures. DISCUSSION Schönlein-Henoch purpura is a generalized vasculitis characterized by skin lesions, joint pain, kidney and gastrointestinal signs. In general, the symptoms are more severe in older children (Watson, 2012). Neurological manifestations may occur occasionally, most are average severity, being represented by headache and behavioral disorders. Severe neurological symptoms such as epileptic seizures, peripheral neuropathies and distinct brain hemorrhage are rarely encountered in Schönlein- Henoch purpura (Østergaard 1991, Elinson 1990). The pathogenic substrate of neurological manifestations in Schönlein-Henoch purpura is supposedly represented by cerebral vasculitis lesions. In a 2009 study conducted on a representative sample of 430 children diagnosed with Henoch-Schönlein purpura, Anil and his collaborators reported the presence of neurological signs at 0.7% of cases. Østergaard (1991) reported the presence of focal EEG discharges to more than 50% of children watch with Henoch-Schönlein purpura, even if they had no neurological symptoms. Elinson (1990) noted of neuro-imagistic examination the presence of cerebral ischemia signs in patients with Henoch- Schönlein purpura. In a small number of cases in patients with Henoch-Schönlein purpura and epileptic seizures has been reported the presence of brain hemorrhage at neuro-imaging examination which is due to the brain vasculitis who was attributed to reducing the level of prothrombin and XIII factor (Mirsa 2004, Karamadoukis 2008). Both cases with Henoch-Schönlein purpura presented in this paper were characterized by concomitant damage at several organs and systems. It is possible that β hemolytic streptococcus have had a potential pathogenic role of those two patients. Neurological symptoms in both situations (epileptic seizures, behavior disorders, headache) started before the appearance of specific skin signs of Henoch-Schönlein purpura. Neuro-imaging exploration was normal in a patient, but at the second were objectified ischemic brain lesion. EEG examination revealed pathological abnormalities from both children. The evolution of patients has been favorable, epileptic seizures were completely controlled by antiepileptic medication. CONCLUSIONS Henoch-Schönlein purpura is a multisystemic condition in which of the clinical picture may be part and neurological signs. Epileptic seizures and behavioral disorders were present in both children evaluated, representing in both cases signs of onset of Schönlein-Henoch purpura. The evolution of neurological manifestations has been favorable, the antiepileptic medication completely controlling the epileptic seizures to both patients.

8 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXI, NR. 4, AN REFERENCES 1. McCarthy H.J., Tizard E.J. Clinical practice: diagnosis and management of Henoch-Schönlein purpura. Eur J Pediatr, 2010; 169(6): Saulsbury F.T. Clinical update: Henoch-Schönlein purpura. Lancet, 2007; 369: Kellerman P.S. Henoch-Schönlein purpura in adults. Am J Kidney Dis, 2006; 48: Brogan P.A. What s new in the aetio-pathogenesis of vasculitis? Pediatr Nephrol, 2007; 22(8): Bakkaloğlu S.A., Ekim M., Tümer N. et al. Cerebral vasculitis in Henoch-Schönlein purpura. Nephrol Dial Transplant, 2000; 15: Watson L., Richardson A.R.W., Holt R.C.L. et al. Henoch-Schönlein purpura a 5-year review and proposed pathway. PLoS ONE, 2012; 7(1): Østergaard J.R., Strom K. Neurologic manifestations of Henoch- Schönlein purpura. Acta Paediatr Scand, 1991; 80: Elinson P., Foster K.W., Kaufman D.B. Magnetic resonance imaging of central nervous system vasculitis. A case report of Henoch-Schönlein purpura. Acta Paediatr Scand, 1990; 79: Anil M., Aksu N., Kara O.D. et al. Henoch-Schönlein purpura in children from western Turkey: a retrospective analysis of 430 cases. The Turkish Journal of Pediatrics, 2009; 51: Misra A., Biswas A., Das S.K. et al. Henoch-Schönlein purpura with intracerebral haemorrhage. JAPI, 2004; 52: Karamadoukis L., Ludeman L., Williams A.J. Henoch-Schönlein purpura with intracerebral haemorrhage in an adult patient: a case report. Journal of Medical Case Reports, 2008; 2:

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